We study maternal effects on the immune system and development of allergic diseases, with a particular focus on asthma. Maternal effects are defined as influences of maternal environment, genotype or phenotype on the phenotype of the offspring. Maternal effects have been observed in a number of species, including mice and humans, for several environmental factors and in several tissues and systems of the offspring, including their immune system. Maternal effects may be beneficial, increasing offspring adaptation to changes in the environment and preventing a disease, and harmful, leading to a disease. List of maternally-influenced diseases includes asthma.  The existence of maternal effects in asthma has been hypothesized because 1) asthma frequently starts in the first years of life, 2) aberrant gene variants account for only a small proportion of asthma prevalence (GWAS and rare variant studies), 3) childhood asthma associates with maternal environmental exposures and health status. Harmful maternal exposures and phenotypes with positive associations with childhood asthma include road traffic-related air pollution, cigarette smoke and maternal stress. Maternal environmental factors with negative association with childhood asthma include certain microorganisms, and in particular, bacteria present in the farming environment. The overarching goal of our laboratory is to delineate mechanisms underlying maternal effects on asthma. More specific goals are to define maternal information that is transferred to offspring, or lost and not transmitted to offspring, elucidate routes of information transfer (placenta, breast milk, gametes), delineate offspring cells and pathways that are programmed by this information, and study how these cells and pathways contribute to the development of asthma. We have particular interest in cells and pathways of the immune system. The translational goals are to identify early-life biomarkers of predisposition to asthma in humans and define molecular targets for development of preventive drugs.     

 

Lab Resources & Services

Lab location:
National Jewish Health
Goodman Building, room K613
1400 Jackson St
Denver, CO 80206

Contact:
Magdalena M Gorska (PI)
Email: GorskaM@NJHealth.org
Lien Hang (Administrative Assistant)
Email: HangL@NJHealth.org
Phone number: 303.398.1656
 

Methods

  • Mouse models of asthma
  • Mouse models of prenatally-induced predisposition to asthma
  • Analysis of neonatal mice
  • Dissection and analysis of embryonic organs and placentas
  • Isolation of immune cell subsets from mouse tissues and human peripheral blood
  • Immune cell transfer approaches
  • In vitro assays to study activation of immune cells
  • Multi-color flow cytometry
  • Confocal microscopy
  • Molecular biology, including gene cloning, site-directed mutagenesis, mammalian cell transfection, generation of recombinant retroviruses and retroviral infection, protein expression and purification
  • Assays to study activation of signaling molecules
  • RNA-seq 

 

Current Projects & Grant Information

To begin addressing our goals, we developed a mouse model, inducing asthma susceptibility in young mice by exposing their mothers to diesel exhaust particles (DEPs). Learn More

 

Personnel

Principal Investigator
Magdalena M Gorska, MD, PhD

Magdalena Gorska is a Training Faculty Member of the Immunology Graduate Program at the University of Colorado, Aurora, CO.

Postdoctoral Research Associates

Administrative Assistant

Training & Job Opportunities

Our lab has openings for a postdoctoral research associate and a lab researcher.

We also welcome motivated graduate students to do rotation and/or join our lab. 
 

 

Publications

  • Qian Q, Chowdhury BP, Sun Z, Lenberg J, Alam R, Vivier E, Gorska MM. Maternal diesel particle exposure promotes offspring asthma through NK cell-derived granzyme B [published online ahead of print, 2020 Jun 29]. J Clin Invest. 2020;130324. doi:10.1172/JCI130324. PMID: 32407293

  • Lenberg J, Qian Q, Sun Z, Alam R, Gorska MM. Pre-pregnancy exposure to diesel exhaust predisposes offspring to asthma through IL-1β and IL-17A. J Allergy Clin Immunol. 2018, 141:1118-1122.e3. PMCID: PMC5844783.

  • Manners S, Alam R, Schwartz DA, Gorska MM. A mouse model links asthma susceptibility to prenatal exposure to diesel exhaust. J Allergy Clin Immunol. 2014, 134:63-72.e7. PMCID: PMC4065237.

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